Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

被引:41
作者
Xie, Yunjie [1 ]
Zhang, Haitao [1 ]
Zhang, Yang [1 ]
Wang, Chong [1 ]
Duan, Deyi [1 ]
Wang, Zheng [1 ]
机构
[1] Jining First Peoples Hosp, Dept Neurosurg, 6 Jiankang Rd, Jining 272011, Shandong, Peoples R China
关键词
Spinal cord injury; Chinese angelica polysaccharide; apoptosis; inflammation; COX-1; SPINAL-CORD-INJURY; SIGNAL-TRANSDUCTION; SINENSIS; CYCLOOXYGENASE-1; ACTIVATION; PI3K/AKT; RELEASE;
D O I
10.1159/000493415
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI). Methods: PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and a poptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway. Results: LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1p, IL-6, IL-8, and TNF-a were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner. Conclusion: CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via downregulation of COX-1. (C) 2018 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:1380 / 1388
页数:9
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